Evidence map›Paper›PMID 30729269›Full record

ReviewHerz2019

Critical inflammatory mechanisms underlying arrhythmias.

N Vonderlin, J Siebermair, E Kaya, M Köhler, T Rassaf, R Wakili

Abstract readReview
PubMed Publisher
In one paragraph

Review in Herz, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  3. Immune Regulation in Atrial Cardiomyopathy.Reviews in cardiovascular medicine · 2025
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  6. Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

N VonderlinKlinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum Essen, Universitätsklinikum der Universität Essen, Hufelandstr. 55, 45147, Essen, Germany.
J SiebermairKlinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum Essen, Universitätsklinikum der Universität Essen, Hufelandstr. 55, 45147, Essen, Germany.
E KayaKlinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum Essen, Universitätsklinikum der Universität Essen, Hufelandstr. 55, 45147, Essen, Germany.
M KöhlerKlinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum Essen, Universitätsklinikum der Universität Essen, Hufelandstr. 55, 45147, Essen, Germany.
T RassafKlinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum Essen, Universitätsklinikum der Universität Essen, Hufelandstr. 55, 45147, Essen, Germany.
R WakiliKlinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum Essen, Universitätsklinikum der Universität Essen, Hufelandstr. 55, 45147, Essen, Germany. reza.wakili@uk-essen.de.
West German Heart and Vascular Center Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the past few decades, cardiovascular research has increasingly focused on systemic inflammatory mechanisms, particularly in the field of atherosclerosis but also in association with cardiac arrhythmogenesis. Objective inflammatory markers including C‑reactive protein and cytokines, also called "biomarkers," seem to serve as predictors of onset and prognosis of cardiac arrhythmias. This review gives an overview of potential mechanisms underlying inflammatory processes and arrhythmias, especially atrial fibrillation, which is the most common sustained arrhythmia in daily clinical routine. The association between inflammatory pathways and cardiac arrhythmia is highly complex and includes direct as well as indirect pathways. While past research into arrhythmia focused on fibrosis, altered action potential properties, and ischemia, novel concepts include coagulation and inflammation in cardiac tissue. The underlying mechanisms are altered electrophysiological properties, including ion channel disturbance, early and late afterdepolarizations, as well as enhanced fibrosis and structural remodeling in cardiomyopathies. These pathophysiological factors favor the occurrence of ectopic pacemakers as well as re-entry tachycardia. Further studies are essential to better understand the main inflammatory signal cascades and the exact proarrhythmic effect of interacting key mediators. This will facilitate the evaluation of future anti-inflammatory therapeutic approaches for arrhythmias, analogous to recent developments in atherosclerosis.

Indexed as

Atrial FibrillationInflammationTachycardiaFibrosisHumansAtherosclerosisAtrial fibrillationCardiac arrhythmogenesisC-reactive proteinCytokines

Identifiers

PMID30729269
OpenAlexW2912836197

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.